Postsynaptic firing produces long-term depression at inhibitory synapses of rat visual cortex.

High-frequency activation of excitatory synapses produces long-term depression (LTD) at inhibitory synapses in rat visual cortex. The LTD generation mechanism was studied by recording inhibitory postsynaptic potentials from layer V cells in response to layer IV stimulation under pharmacological blockade of excitatory synaptic transmission. LTD occurred after depolarizing current pulses applied to postsynaptic cells elicited repetitive firing. LTD induction was facilitated by a bath application of an L-type Ca(2+) channel activator, 1,4-Dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl) phenyl]-3-pyridinecarboxylic acid, methyl ester (BAY K 8644), while it was prevented by either the bath application of L-type Ca(2+) channel blocker nifedipine or postsynaptic loading of Ca(2+) chelator 1,2-bis-(o-aminophenoxy)ethane-N,N,N',N',-tetraaceticacid (BAPTA). These results suggest that LTD induction is at least partly mediated by Ca(2+) entry through L-type Ca(2+) channels in association with postsynaptic action potentials.